8) Infectious Disease (Part 2) Flashcards

1
Q

TB transmission

A
  • Person to person by droplet nuclei

- Aerosolized by coughing, sneezing or speaking

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2
Q

TB infectivity correlates

A
  • Concentration of organisms in expectorated sputum
  • Extent of pulmonary disease
  • Frequency of cough
  • Intimacy & duration of contact
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3
Q

Pathophysiology of TB

A
  • Aerosolized droplets enter lungs
  • Tubercle Bacilli reach the alveoli and are ingested by alveolar macrophages
  • In most individuals, M. tuberculosis infection is contained initially by host defenses, and infection remains latent
  • Infection occurs if the inoculum escapes alveolar macrophage microbicidal activity
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4
Q

Latent TB infection

A
  • T cells and macrophages surround the organisms in granulomas that limit their multiplication and spread
  • These people do not have active disease and cannot spread the disease to others
  • Clinically asymptomatic
  • CXR is negative
  • The only evidence of infection may be a reaction to the tuberculin skin test or positive interferon gamma release assay (IGRA)
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5
Q

Increased risk populations for TB

A
  • Contacts of persons to have suspected or confirmed TB
  • IV drug users
  • Foreign born persons who recently arrived from a country with high TB incidence
  • Health care workers who serve high-risk patients
  • Residents and employees of high risk settings (correctional institutions, nursing homes, mental institutions, homeless shelters)
  • Children and adolescents exposed to adults in high-risk categories
  • Medical risk factors that increase the risk for TB (i.e. silicosis, HIV infection, CKD, leukemia, lymphoma, DM, unintentional weight loss, patients receiving immunosuppressive therapy etc.)
  • Mycobacteriology laboratory personnel
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6
Q

Screening for latent TB

A
  • Tuberculin skin test (TST) Or the interferon gamma release assay (IGRA)
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7
Q

Reading the Tuberculin Skin Test (Mantoux test of purified protein derivative/PPD)

A
  • Measure reaction in 48 to 72 hours
  • Measure induration (not erythema)
  • Record reaction in millimeters, not “negative” or “positive”
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8
Q

Tuberculin skin test false positives

A
  • Previous BCG vaccination
  • Infection with nontuberculosis mycobacteria
  • Incorrect method of TST administration
  • Incorrect interpretation of reaction
  • Incorrect bottle of antigen used
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9
Q

Tuberculin skin test false negatives

A
  • Cutaneous anergy (anergy is the inability to react to skin tests because of a weakened immune system…such as HIV/AIDS)
  • Recent TB infection (within 8-10 weeks of exposure)
  • Very old TB infection (many years)
  • Very young age (less than 6 months old)
  • Recent live-virus vaccination (e.g., measles and smallpox)
    Overwhelming TB disease
  • Some viral illnesses (e.g., measles and chicken pox)
  • Incorrect method of TST administration
  • Incorrect interpretation of reaction
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10
Q

interferon-gamma release assay (IGRA) tests for TB infection

A
  • Blood Tests (must be processed within 8-16 hours after collection)
  • Only one visit to health care provider to draw the blood
  • Results can be available in 24 hours
  • Results are not affected by prior (bacille Calmette-Guérin) BCG vaccination
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11
Q

Blood tests for TB

A
  • Must be processed within 8-16 hours after collection
  • QuantiFERON®-TB Gold test (QFT-G)
  • QuantiFERON®-TB Gold In-Tube test (GFT-GIT)
  • T-SPOT®- TB
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12
Q

Latent TB infection test results

A
  • Positive Tuberculin skin test OR Positive QFT blood test
  • Negative chest radiograph
  • No symptoms or physical
    findings suggestive of TB
    disease
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13
Q

Pulmonary TB disease test results

A
  • Tuberculin skin test or QFT (QuantiFERON-TB/QuantiFERON-Gold) blood test positive
  • Chest radiograph may be abnormal
  • Symptoms may include one or more of the following: fever, cough, night sweats, weight loss, fatigue, hemoptysis, decreased appetite
  • Respiratory specimens may be smear or culture positive
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14
Q

Why treat latent TB?

A
  • Reactivation possible
  • Active Pulmonary TB Disease may occur in 10% of persons with Latent TB Infection
  • Up to 50% of persons with HIV will develop Active Pulmonary TB Disease within 2 years of infection
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15
Q

Other conditions associated with increased incidence of developing Active Pulmonary TB Disease

A
  • Silicosis
  • DM
  • Patient taking immunosupressive medications
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16
Q

Tx option for latent infection (negative CXR and no symptoms)

A
  • Once weekly Isoniazide (INH) + Rifapentine x 3 months
  • Daily Rifampin x 4 months
  • Daily INH + Rifampin x 3 months
  • INH x 6-9 months
  • Supplement pyridoxine (vitamin B6) if prescribing INH to avoid peripheral neuropathy side effects
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17
Q

Active Pulmonary TB Disease

A
  • 90% of the time, in adults, represents activation of latent disease
  • Slow Progression of Constitutional Symptoms
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18
Q

Constitutional symptoms (slow progression) of active pulmonary TB disease

A
  • Fever
  • Loss of Appetite
  • Weight Loss
  • Night Sweats
  • Fatigue
  • Cough
  • Blood-streaked sputum
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19
Q

CXR pulmonary TB

A
  • Apical localization is characteristic
  • This localization has been attributed to hyperoxic environment of apices
  • Upper lobe disease marked by irregular reticular & nodular densities
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20
Q

Work-up and diagnosis of TB

A
  • Respiratory isolation for all patients suspected of having Active TB
  • Sputum cultures x 3 for Acid Fast Bacilli (stained smear + AFB confirmed with identification of M. tuberculosis in cultures).
  • Xpert MTB/RIF, a rapid molecular test that accurately diagnoses TB and MDR-TB in 100 minutes
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21
Q

Sputum cultures x 3 for Acid Fast Bacilli in TB patients

A
  • Stained smear + AFB confirmed with identification of M. tuberculosis in cultures
  • Sample must be brought up from a productive cough
    Induced sputum production by inhalation of aerosolized sterile hypertonic saline solution may be performed if pt is unable to produce sputum
  • Bronchoscopy with bronchial washings & bronchoalveolar lavage may be performed if necessary
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22
Q

Mycobacterium bacteriology

A
  • Distinguished by their surface lipids, which cause them to be acid-fast bacilli in lab
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23
Q

Active pulmonary TB Tx

A
  • Do not delay treatment if there is a high clinical suspicion
  • Multidrug regimen (RIPE includes commonly used first-line drugs)
  • Rifampin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
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24
Q

Miliary TB

A
  • Often called “disseminated TB”
  • Due to hematogenous spread & may represent either newly acquired infection or reactivation
  • PPD - 50% of untreated cases & sputum smears - in 80%
    Transbronchial, liver & BM biopsy + in 2/3
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25
Q

Miliary TB signs and symptoms

A
  • Fever, night sweats, anorexia, weakness & weight loss characterize majority of cases
  • Hepatomegaly, splenomegaly, lymphadenopathy, & ocular tubercles may occur
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26
Q

Extrapulmonary TB (rare nowadays because of treatment…however, could occur in HIV/AIDS patients)

A
  • Lymph nodes
  • Pleura
  • GU tract
  • Bones and joints
  • Meninges
  • Peritoneum
  • Any organ system can be affected
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27
Q

HIV transmission

A
  • Anal or vaginal sex
  • Sharing needles, syringes, or other drug injection equipment (cookers)
  • Babies can also get HIV during pregnancy, birth, or breastfeeding
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28
Q

AIDS (stage 3)

A
  • Defined when CD4 cell count drops below 200 cells/mm or the development of certain opportunistic illnesses
  • People with AIDS can have a high viral load and be very infectious
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29
Q

HIV screening guidelines

A
  • U.S. Preventive Services Task Force (USPSTF) upgraded from Grade “C” to Grade “A” recommendation to screen for HIV infection
    in adolescents and adults ages 15 to 65, and also < age 15 to > age 65 who are at risk for infection
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30
Q

Diagnosis of HIV

A
  • 4th generation duo antigen/antibody test
  • Antibodies take 4 weeks to develop
  • P24 antigen and HIV RNA is also tested with 4th generation
  • 10 days after exposed, will now become positive
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31
Q

Routine labs in HIV positive patients (general)

A
  • CBC with Diff
  • CMP (includes Cr. Glucose and LFTs)
  • Lipid Profile
  • TB screen (PPD or IGRA)
  • Pap smear w/ HPV (cervical and/or anal)
  • Gonorrhea and Chlamydia
  • Serologies
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32
Q

Serologies used in routine HIV positive patients (general)

A
  • Toxoplasmosis
  • Cytomegalovirus
  • Varicella IgG
  • Hepatitis A/B/C
  • RPR
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33
Q

Routine labs in HIV positive patients (HIV specific)

A
  • CD 4 Count
  • HIV RNA Assay (viral load)
  • HIV-resistance (genotype)
  • HLA B*5701 (hypersensitivity to Abacavir )
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34
Q

Medications for initial antiretroviral therapy

A
  • Bicteravir/emtricitabine/tenofovir alafenamide (Biktarvy)
  • If B*5701 negative, Dolutegravir/abacavir/lamivudine (Triumeq)
  • Dolutegravir (Tivicay) + emtricitabine/tenofovir disoproxil fumarate (Truvada) or emtricitabine/tenofovir alafenamide fumarate (Descovy)
  • Raltegravir (Isentress) + emtricitabine/tenofovir disoproxil fumarate (Truvada) or emtrictabine/tenofovir alafenamide fumarate (Descovy)
35
Q

HIV disease management ART goals

A
  • Keep viral load as low as possible

- Increase CD4 cell count

36
Q

Prophylaxis is recommended for these diseases

A
  • Varicella-Zoster Virus
  • Pneumocystitis Pneumonia (PCP)
  • Histoplasmosis (if high risk from occupational exposure ir residence)
  • Toxoplasma gondii enceohalitis
  • Mycobacterium avium complex (MAC)
37
Q

Varicella-Zoster Virus prophylaxis

A
  • Any CD4 count
  • Recombinant zoster vaccine (Shingrix)
  • 2 doses 2 months apart
  • Zostavax (zoster vaccine live) is CONTRAINDICATED in AIDS patients (CD4 counts <200)
38
Q

Pneumocystitis Pneumonia (PCP) prophylaxis

A
  • CD4 < 200

- TMP-SMX (Bactrim) or Dapsone (if sulfa allergy)

39
Q

Histoplasmosis prophylaxis

A
  • CD4 count < 150

- Iatroconazole

40
Q

Toxoplasma gondii enceohalitis prophylaxis

A
  • CD4 count < 100

- TMP-SMX (Bactrim) or dapsone (if sulfa allergy)

41
Q

Mycobacterium avium complex (MAC) prophylaxis

A
  • CD4 count < 50

- Azithromycin or Clarithromycin

42
Q

Mycobacterium TB latent infection summary

A
  • TST 5mm or greater or positive IGRA, Negative CXR, Negative Symptoms
  • Treatment: Isoniazid (INH)* and Rifapentine (RPT) x 3 mo, Rifampin (RIF) x 4 mo, INH and RIF x 3 mo or INH* x 6-9 mo
43
Q

Mycobacterium TB active disease summary

A
  • TST 5mm or greater** or positive IGRA, positive CXR, positive symptoms (fever, cough, night sweats, weight loss), positive Sputum for Acid Fast Bacilli
  • Extrapulmonary symptoms with advanced immunosuppression (nodal involvement, CNS, pleural, pericardial, ascites)
  • Treatment: RIPE (plus pyridoxine) or others in CDC guidelines and based on culture and sensitivity report
44
Q

In TB patients, give pyridoxine (vit B6) if using INH to prevent

A
  • Neuropathy side effect
45
Q

Pneumocystitis jirovecii

A
  • Ubiquitous fungus

- Most occur in patients unaware of HIV status or low CD 4 counts

46
Q

Clinical manifestation of Pneumocystitis jirovecii

A
  • Subacute (days to weeks)
  • Progressive dyspnea, fever, non-productive cough, and chest discomfort
  • +/- hypoxia
  • Elevated LDH
  • Spontaneous pneumothorax may occur
47
Q

Pneumocystitis jirovecii CXR

A
  • Diffuse bilateral “ground glass” interstitial infiltrates from the hila in a butterfly pattern or normal
48
Q

Pneumocystitis hirovecii Tx

A
  • TMP-SMX (Bactrim)
49
Q

Neurologic syndromes associated with cryptococcosis

A
  • Subacute meningitis

- Meningoencephalitis

50
Q

Subacute meningitis or meningoencephalitis (cryptococcosis) signs and symptoms

A
  • Fever, malaise, and headache
  • Lethargy, altered mental status, photophobia, neck stiffness
  • Usually disseminated when diagnosed in HIV patient (skin lesions mimicking molluscum contagiosum, pulmonary infections ARDS mimicking Pneumocystitis…any organ can be involved)
  • Ubiquitous in the environment, possible exposure to aged bird droppings may increase risk of infection
51
Q

Subacute meningitis or meningoencephalitis (cryptococcosis) Dx

A
  • CSF shows mild elevation of protein, low-normal glucose, elevated lymphocytes, increased opening pressures
  • Diagnosed with culture, CSF microsocopy, or cryptococcal antigen detection
52
Q

Subacute meningitis or meningoencephalitis (cryptococcosis) Tx

A
  • Amphotericin B plus flucystosine
53
Q

Ring enhancing lesions

A
  • Weakness, seizure fast onset (CNS toxoplasmosis…most common in US) – responds quickly to treatment
  • Weakness, seizure slow onset (lymphoma)
  • Endemic area (TB)
54
Q

Toxoplasmosis (Toxoplasma gondii)

A
  • Reactivation of latent tissue cysts

- Eating undercooked meat, raw shellfish; exposure to cat litter/feces

55
Q

Toxoplasmosis (Toxoplasma gondii) clinical manifestations

A
  • Focal encephalitis (headache, confusion, motor weakness, fever) or non-specific headache and psychiatric symptoms
56
Q

Toxoplasmosis (Toxoplasma gondii) Tx

A
  • Pyrimethamine plus sulfadiazine (clindamycin in sulfa allergy) plus leucovorin
57
Q

Progressive Multifocal Leukoencephalopathy (PML)

A
  • Major opportunistic infection causing reactivation of the John Cunningham (JC) virus
  • May occur shortly after initiation of ART due to immune reconstitution inflammatory syndrome (IRIS)
58
Q

Progressive Multifocal Leukoencephalopathy (PML) clinical manifestations

A
  • Altered mental status
  • Visual changes
  • Ataxia
  • Seizures
59
Q

Progressive Multifocal Leukoencephalopathy (PML) imaging

A
  • Multifocal process limited to the white matter
60
Q

Progressive Multifocal Leukoencephalopathy (PML) Dx

A
  • Brain biopsy
61
Q

Progressive Multifocal Leukoencephalopathy (PML) Tx

A
  • ART to restore immune system

- Adding high dose glucocorticoids if evidence of brain swelling due to immune response inflammatory syndrome (IRIS)

62
Q

Progressive Multifocal Leukoencephalopathy (PML) prognosis

A
  • Often fatal
63
Q

CMV retinitis

A
  • Most common clinical manifestation of CMV in HIV patients

- Usually starts as unilateral, but can progress to bilateral if not treated

64
Q

CMV retinitis presentation

A
  • May be asymptomatic or present with floaters, scotomata, or peripheral visual field defects
  • Full-thickness necrotizing retinitis, with classic “fluffy yellow-white” retinal lesions with or without intraretinal hemorrhage
65
Q

CMV retinitis Tx

A
  • IV ganciclovir followed by oral valganciclovir
66
Q

Other HIV presentations

A
  • CMV polyradiculoapthy (saddle paresthesias, asymmetiric lower extremity weakness, bowel dysfunction)
  • Emergency…diagnosed via CMV culture of CSF and TX
67
Q

Shingles in young pt (25% chance this is HIV) Tx

A
  • Antivirals & pain meds
  • Acyclovir, valacyclovir, or famciclovir
  • Hospitalization with IV acyclovir if disseminated
  • Emergent ophthalmic referral if involving trigeminal (V1)
68
Q

Kaposi’s sarcoma

A
  • Human Herpes Virus 8
  • Transmission most likely via oral (kissing)
  • Red-Purple papular lesions and plaques, nodules with edema (similar to Bacillary Angiomatosis)
69
Q

Kaposi’s sarcoma Tx

A
  • TX with ART, others may need low dose chemotherapy
70
Q

Risk of transmission from a single percutaneous needle stick or cut with a scalpel from an infected patient

A
  • Hepatitis B is about 6-30%
  • Hepatitis C is about 1.8%
  • HIV is about 0.3%
71
Q

Factors that increase the riskof exposure to body fluids

A
  • Failure to adopt universal precautions
  • Not following established a protocol of safety
  • Performing high-risk procedures that increase the risk of blood exposure
  • Using needles and other sharp devices that lack safety features
72
Q

What should be the first response to a percutaneous exposure?

A
  • Wash the area thoroughly with soap and water
  • Punctures and small lacerations could be cleaned with alcohol based hand solution
  • Mucous membranes should be extensively irrigated with water or saline
73
Q

Second response to percutaneous exposure (after cleaning)

A
  • Report the exposure and obtain Hepatitis and HIV screening for both the provider and the source patient (per protocol of institution) and discuss need for post-exposure prophylaxis
74
Q

What are the indications for HIV Post Exposure Prophylaxis (PEP)?

A
  • A percutaneous, mucous membrane, or nonintact skin exposure to blood or bloody body fluids of a patient with known HIV infection
  • If HIV status of the source patient is unknown & if the source has risk factors for HIV infection (injection drug users, men who have sex with men) or symptoms suggesting HIV infection & you are waiting for HIV testing
75
Q

When should HIV PEP start?

A
  • As soon as possible! Less than 2 hours after exposure give a “starter pack” (don’t wait for HIV results if they are not back yet!)
  • If more than 72 hours, most should not get PEP
  • If it is a very high-risk exposure (sharps injuries from a needle that was in an artery or vein of an HIV-infected source patient), PEP can be offered up to one week after the exposure
76
Q

What PEP meds should be used (3-drug regimen)?

A
  • tenofovir DF 300 mg and fixed dose combination
  • emtricitabine 200 mg (Truvada) once daily

with

  • raltegravir (Isentress) 400 mg twice daily

or

dolutegravir (Tivicay) 50 mg once daily

77
Q

How long should PEP be taken?

A
  • 4 weeks

Discontinue if source patient is shown to be negative

78
Q

Hepatitis B prophylaxis if the healthcare provider is already vaccinated and patient is HBsAg positive

A
  • Check an anti-HBs level in the healthcare worker
  • If the post-vaccination anti-HBs level is high (greater than 10 mIU/mL), this is known to beprotective, and there is no need for further treatment, and a booster shot is not recommended
  • If the post-vaccination anti-HBs titer is low, the healthcare worker should be administered hepatitis B immunoglobulin
79
Q

Hepatitis B prophylaxis if the healthcare provider is already vaccinated and patient is HBsAg negative

A
  • Observe the healthcare worker and monitor anti-HBs levels
80
Q

Hepatitis B prophylaxis if the healthcare provider is already vaccinated if patient has been discharged or not available for testing

A
  • Most infectious disease experts treat such cases as if the source was HBsAg negative unless the source has a high risk for HBV infection (such as current or former IV drug use)
  • In this case, the assumption is made that the patient is HBsAg positive, and Post-exposure prophylaxis is initiated
81
Q

Hepatitis B prophylaxis if the healthcare provider is NOT vaccinated and patient is HBsAg positive

A
  • The healthcare worker should be administered HBV immunoglobulin immediately, followed by a rapid course of active immunization starting 14 days later
82
Q

Hepatitis B prophylaxis if the healthcare provider is NOT vaccinated and patient is HBsAg negative

A
  • No need to administer hepatitis B immunoglobulin

- Healthcare worker should strongly be recommended to get the Hepatitis B vaccine

83
Q

Hepatitis B prophylaxis if the healthcare provider is NOT vaccinated and patient is not available for testing

A
  • If there is any suspicion about the patient’s clinical status, workers must be offered Hepatitis B immunoglobulin, and active vaccination should be recommended in 14 days time